A Case of Torsade de Pointes Associated with Hypopituitarism due to Hemorrhagic Fever with Renal Syndrome

We describe a 51-yr-old man presenting with syncope due to torsade de pointes. The torsade de pointes was refractory to conventional medical therapy, including infusion of isoproterenol, MgSO4, potassium, lidocaine, and amiodarone. His past history, physical findings, and hormone study confirmed that QT prolongation was caused by anterior hypopituitarism that developed as a sequela of hemorrhagic fever with renal syndrome. The long QT interval with deep inverted T wave was completely normalized 4 weeks after starting steroid and thyroid hormone replacement. Hormonal disorders should be considered as a cause of torsade de pointes, because this life-threatening arrhythmia can be treated by replacing the missing hormone.

Torsades de Points: análise de 105 episódios / Torsades de Pointes: analysis of 105 episodes

Purpose - To analyze episodes of Torsades de Pointes (TP), in search of its electrocardiographic characteristics. Patients and Methods - We analyzed 105 episodes of TP, in 4 patients using quinidine and diuretics, recorded by 24-hour Holter monitoring The following parameters were studied; ventricular repolarization out of TP, rhythm disturbances before TP; EKG characteristics of the onset, the bouts and the end of the TP. Results - Ventricular repolarization, out of the TP, was abdormal, with the presence of U-waves at the end of the T-waves, resulting in prolongation of the QT (QU) interval. The U-wave voltage was noted to be cycle-lenght dependent. Ventricular bigeminy preceded TP in 100 episodes (95%) and the mean interval between both parameters was 18 ±16 min. The onset of the TP episodes showed the "short/long/ short cycle rale", hereby called "pre-pause cycle", "preparing cycle" and "trigger cycle" respectively. The rotatory QRS-T morphology around the baseline, was seen in 75% of episodes, at the beginning or throughtout the bout. Monomorphic ventricular tachycardia pattern was seen in the other 25% of episodes. Termination of bouts was sudden in all cases, and persistent ventricular bigeminy led to another bout in 90 episodes (85% ). Conclusion - In TP patients, there is enlargement of QT intervals mostly due to U-waves appearence. The U-waves seen in these cases, probably have an important role in the genesis of TP and are probably related to ventricular after potentials (triggered activity). Ventricular bigeminy is a premonitory sign of TP in patients using class 1A antiarrhythmic drugs Persistent ventricular bigeminy post-TP episoaes is a strong indicator of another bout of TP. The onset of TP is more important than its morphology for the correct diagnosis of this arrhythmia